CHANGES IN BODY COMPOSITION IN ACUTE RENAL FAILURE

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CHANGES IN BODY COMPOSITION IN ACUTE RENAL FAILURE

L. W. Bluemle Jr., … , H. P. Potter, J. R. Elkinton

J Clin Invest. 1956;35(10):1094-1108. https://doi.org/10.1172/JCI103364.

Research Article

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CHANGES IN BODY COMPOSITION IN ACUTE RENAL FAILURE'

By L. W. BLUEMLE, JR.,2 H. P. POTTER, AND J. R. ELKINTON8

(From ^the Chemical Section of the Department of Medicine, University of Pennsylvania, School of Medicine, Philadelphia, Penna.)

(Submitted for publication April 9, 1956; accepted June 11, 1956) To a large degree the therapy of acute renal

failuredependson anunderstanding ofbiochemical disturbances that result from the temporary ab- senceof renalexcretory and homeostatic functions.

Important among these disturbances are changes in thevolume andcomposition of body fluids, particularly with respect to electrolyte constituents.

While certain manifestations of these changes are frequently recognized on the clinical level, relatively little quantitative data are available from which can be derived a general pattern of body fluid alterations in this disease. One reason for this paucity of information, aside from the limita- tions of investigative techniques, is the inherent difficulty of performing adequate studies on critically ill patients.

Sirota and Kroop (1) observed in 4 oliguric patientsanexpansion ofinulin space roughly com- mensurate with estimated positive fluid balance.

They postulated that the oliguric phase of acute renal failure is associated with cellular dehydra- tion resulting from a shift of water out of cells, and that hyponatremia may result in part from extracellular dilution and in part from a shift of sodium into cells. The observation by Schwartz, Tomsovic,and Schwartz (2) of greater expansion of inulin space than of D20 space in one anuric child would conform with this concept. Iseri, Batchelor, Boyle, and Myers (3) also suggested that the hyponatremia and hypochloremia of oliguria may be due in part to cellular uptake of sodium and shift of water from cells to extracellular fluid.

1 This study was aidedby grants from The American Philosophical Society, The National Heart Institute of the U.S.P.H.S. (H-340), andtheC. Mahlon KlineFund of the Departmnent ^of Medicine, University of Pennsyl- vania.

2J. Allison Scott Fellow of the Departnent of Re- search Medicine (1953-55); Markle Scholar in Medical Science 1955-56.

8Established Investigator of The American Heart Association.

The role ofcatabolism inaugmenting total body water through water of oxidation and release of preformedwater wasevaluatedbyHamburger and Richet (4), largely by inference from observations made during post-oliguric diuresis. Changes in the volume and distribution of body water were also studied in anuric dogs by Hamburger and Mathe (5), who found close agreement between the expansion of total body water as measuredby D20spaces and the amount of water derivedfrom metabolic processes. On the basis of extensive clinical observation and a limited number of iso- topic dilutionstudies, Merrill (6) has enumerated some of the fluid and electrolyte changes frequently seen in prolonged acute renal failure, as follows: 1) an increasein total bodywater, 2) an increase in total body sodium with a decreasing serum concentration, 3) a decrease in total body potassium withanelevated serumlevel, and4) an increased extracellular fluid volume.

Theprimary purpose of the present study was to obtain more complete information concerning the type andmagnitude ^ofchanges in volumeand electrolyte compositionof body fluids in acute re- nalfailure,to assessthe roles of catabolicprocesses andconcomitant fluidtherapyintheirgenesis,and todelineate certaintherapeutic implications^of^this information.

EXPERIMENTAL MATERIAL AND METHODS

Eight patients ^with acute renal failure were studied by the balance technique on the Metabolic Unit ^{of the} Hospital of the University of Pennsylvania. Studies were initiated in 13 patients but were interrupted or in- validated in 5 for various reasons. Measurements ^were made of intake of water, solids, chloride, sodium, ^potassium, nitrogen,ând carbohydrate ând fat, ^{and of all} ôut- put of water, solids, chloride, sodium, potassium, ^{and ni-}

trogen. At the beginning and end of each unit balance period (24 ^to 72 hours) body weight ^was ^obtained ^{on a} stretcher-scale (7) ^and ^blood ^was ^drawn ^for ^determina- tions of serum chloride, sodium, potassium, ^CO2 ^con-

tent, and blood urea nitrogen. Chemical methods of these analyses have been previously ^described (8). ^On 1094

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CHANGES IN BODY COMPOSITION IN ACUTE RENAL FAILURE

TABLE I

Summary ofclinical material

Dayof

Body Dura- Dura- dialysis

surface tion of tionof (from

area* Apparentcauseof acute oliguria study onsetof

Patient Age Sex (sq. mekrs) renal failure Complicatingfactors (days) (days) oliguria) Result

V.N. 42 F 1.82 Hemolyticreactionto Acuteparotidabscess 12 24 7 Recovered 1000ml.incompatible during diuretic phase

blood during hyster- ectomy

E.G. 41 F 1.59 Hemolyticreactionto Pelvicperitonitis,con- 12 22 7 Recovered 2000ml.incompatible vulsions during diure-

blood during hyster- tic phase ectomy

B.S. 26 F 1.55 Septicabortion Peritonitis, pelvic^ab- ¹² ¹⁵ ¹⁰ Recovered

scess, GIhemorrhage, chemical pericarditis, pul. congestion

K.B. 42 F 1.73 Hemolyticreactionto Convulsions during ¹⁴ ¹⁹ 8 Recovered

2000ml.incompatible diuretic phase bloodduring cholecys-

tectomy

I. T. 60 F 1.72 Hypotension during Hemorrhagefrom op- 17 22 8 Recovered

facialsurgery for car- erative site during

cinoma diuretic phase

M. G. 43 F 1.89 Hypotension ^follow- Pulmonary edema,po- 9 3 None Died

inghysterectomy tassium intoxication

F.B. 58 F 1.47 Hypotension during Shockfollowingdialy- 10 12 9 Recovered cardiac surgery sis

D.S. 24 F 1.74 Postpartumshockand Convulsions during ¹⁰ ¹⁴ ⁹ Recovered

hemolytic reaction to diuretic phase 500 ml. incompatible

blood

*Surfaceareain sq. meters ⁼

Wt.°

^{X Ht.07} ^X^0.007184 ^(afterDuBois and DuBois

[15]).

completion ofeachstudythe observed data^wereanalyzed for each unit balance period and recorded for the sake of convenience as average values per 24 hours for each of the following three phases: I) the oliguric phase (urine volume less than 400 ml. per 24 hours), II) ^the early diuretic phase (urine volume 400 ml. per 24 hours tomaximal diuresis),and III) late diuretic phase (maxi- maldiuresis toendofstudy). In allexceptone case (M.

G.) balance studies were continued until the patient ^was ambulatory and was receiving ^no special therapy. It should be clearly pointed ^out that balance studies were not inititatedatthe onset ofoliguria in any of these patients, the average interval being 8.4 days, ^the shortest 5 days, between onset ofoliguria and beginning of studies. Hence the cumulative data relating to Phase I should not be considered representative of metabolic changes during the entire oliguric period.

Brief clinical summaries of each case are presented in Table I. All patients were transferred from other hos- pitals in either the latter part of the oliguric phase or theearly diuretic phase. Duration of study ranged from 3 to 24 days (average 16.4 days). Four patients were studied during Phases I, II, and III; two during only

Phases II andIII;oneduring only Phases I and II, and oneduring onlyPhase I. All patients were critically ill atthe time of transfer, and all except one (M. G.) were treated by extracorporeal hemodialysis prior to initiation of balance studies.4 No attempt was madeto determine the effect of dialysis on subsequent fluid and electrolyte balance; however, the predominant effect as judged by improvement in serum electrolyte pattern and, in some cases, loss of excess body water (by ultrafiltration) was to compensate partially for the fluid and electrolyte disturbances which had occurred up to that time.

Therapy prior to transfer to our hospital varied con- siderably from patient to patient. In almost all cases littleattempt had been made to restrict fluid intake during theearlydays of oliguria; in 3 patients (B. S., I. T., and M. G.) signs ofoverhydration wereevident on admission.

Fluid therapy during this study, presented as average intake figures in Table II, followed generally accepted principles of attempting to prevent or correct the more 'In one case (K. B.) dialysis was performed on the third day of study, and this day was omitted from the calculations.

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J.

serious fluid and electrolyte disturbances as judged by clinical observations and serum studies. Balance data were not used as the primary criteria for judging subsequent fluid therapy. During the oliguric phase intake was limited to an average of 1,000ml.per day, or roughly 700 ml. plus previous 24-hour measured water loss, except in one case (M. G.) where pulmonary edema neces- sitated more drastic fluid restriction. Electrolyte intake was also limited during this phase because of minimal output. Both water and electrolyteintake were increased during Phases II and III to compensate for increasing urinary losses.

CALCULATIONS

Changes in the composition of the body and in certain constituents of the body fluids may be calculated from the data obtained by the balance technique as described above. Although most of these derivations have been in use for many years, the equations which were used in this study are presented here in order that our analysis may be clearly understood. The validity of the data so derived is taken up subsequently under Discussion.

Metabolic mixture

Carbohydrate burned (C) was assumed to be equivalent to the carbohydrate administered.

Protein burned (P) in grams was calculated from the nitrogen excretion in the urine (UVN) in grams corrected for changes in the amount of the urea nitrogen in the body fluids (ABUN) in grams:

P=6.25X (UVN+ABUN). (1)

This latter correction, a proportionately large one in the severely oliguric patient, was made by multiplying the change in concentrationofbloodureanitrogen(A[BUN] ), in grams per liter, by anassumed volume for total body water (W) inliters:

ABUN=A[BUN] XW. (2)

Since change in the lastfactor,W, isoneobjective of the calculation, a series of approximations beginning with a total body water assumedtobe 73.2 per cent of thelean bodymass at theend of the study, permits a reasonable calculation of this portion of theprotein burned.

Fat burned (F) was calculated from the insensible weight loss (IL) and the carbohydrate and protein burned, according^to theformula of Lavietes (9):

F⁼ (IL-2.12 C-1.69 P) /3.79, ₍₃₎ where

IL⁼(Wt. intake -Wt. output) ^- AWt. (4) Change in body composition

Changeinbody fat (ABF) ^wastaken ^asthe difference betweentheexogenousfatgiven (F..) and the fatburned

(F):

ABF=F..-F. (5)

Changein totalbodywater (AW) ^was^calculated ^from the change inweight (AWt) correctedfor the balance of

solids

(Sexereta

^-

Singesta)

and the metabolic mixture (10):

AW=AWt+ (S.-St) +(C+F+0.54 P). (6) Change in total body solids (ABS) was taken as:

ABS=A&Wt- (ABF +AW). (7) Change in lean body mass (ALBM) was obtained as:

ALBM⁼AWt-ABF or

=AW + ABS.

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(9) In addition, absolute amounts of the principal body components were estimated in each patient at the end of the study when the body constituents presumably had returned to or toward normal proportions. Lean body mass (LBM) was calculated in all but one case (M. G.) from the excretion rate of creatinine (UVcr) during the last2 or 3 days (when the plasma creatinine had fallen to essentially normal levels), by the formula of Miller and Blyth (11):

LBM=20.97+0.5161UVer, (10) where UV,r is the excretion rate of creatinine in milli- grams per hour, corrected for any change in plasma level (in the same manner as UVN is corrected in Equation 2 above). Given theestimated lean bodymass, total body fat (BF), total body water (W), and total body solids

(BS) arecalculatedas:

BF=WT-LBM, W=0.732 LBM, BS=LBM-W.

(11) (12) (13) Given these absolute values, changes in total body fat, water, and solids were readily calculated backward in time from the end of the study by using the values for changes derived inEquations 5, 6,and 7 above.

Change in extracellular fluidvolume (,AEa,),asequated with thechloride space, wascalculated from the chloride balance in the usual manner (12) and change ^{in intra-} cellular fluid (AI) was taken as the difference between AW andAEai. For purposesofcalculation ofpercentage changes the total extracellular water at the end of the study was assumed to be 22.5 per cent of the lean body mass.

Electrolyte exchanges

Changes in extracellular sodium and potassium (ANan

and AKu) and in intracellular sodium and potassium (ANa, and AKO) ^were ^calculated ^{on the} ^{basis of} ^the

chloride space in the usual manner as described in Equa- tions 20 to 23 inclusive in Elkinton ^and Danowsli (13).

Transfers of intracellularpotassium ⁱⁿêxcess ôfnitrogen (AK,') were calculated on the assumption ôf â ^normal

K: N ratio of 3.0 mEq. to 1 gm. Electrolyte ^losses through sweatwere not includedin the calculations, ^this

lossbeing considered insignificant ^{since the} patients ^were

kept inair-conditioned rooms.

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TABLE III

Observeddata:body weights,totalbalancesofelectrolytesandnitrogen,concentrationsof

electrolytesin serumandof^bloodureanitrogen

Day from Totalbalance* Serumconcentration Blood

onsetof Body urea

Patient oliguria Cl Na K N weight Cl Na K C02 nitrogen

mEq. mEq. mEq. mM. mg.per

mEq. mEg. mEq. ^gm. kg. Per L. Per L. perL. perL. 100ml.

V.N. 8 79.43 97 139 5.1 28.7 81

12 -109 -106 - 22 - 7.5 79.08 92 133 5.2 21.8 118

20 -256 -374 -213 - 87.4 72.48 91 138 4.0 25.0 148

32 -133 -177 -156 -124.8 68.50 100 139 4.0 31.0 11

E. G. 8 61.96 88 133 3.9 30.2 66

12 - 92 - 32 - 25 - 6.3 62.21 77 128 3.9 27.6 114

21 -119 -386 - 73 - 64.4 55.04 87 136 4.9 25.5 82

30 +309 + 66 -178 - 59.9 53.76 103 141 4.8 21.7 15

B. S. 11 59.50 122

12 - 16 - 25 - 22 - 2.8 59.47 88 138 4.8 24.6 142

19 -440 -550 -203 - 68.2 55.04 76 131 3.5 25.4 180

26 +232 -100 - 56 -118.9 51.66 105 140 4.0 25.8 33

K. B. 5 63.70 93 134 4.7 17.5 120

14 -124 -196 -170 - 10.4 60.01 91 136 5.4 14.9 175

21 -247 -180 -298 - 84.4 57.14 91 136 3.7 30.0 116

24 + 39 - 72 - 18 - 43.9 57.03 90 135 3.8 29.3 70

I.T. 9 68.42 100 146 5.6 28.3 36

17 - 81 -118 + 3 - 7.5 66.84 94 141 6.3 20.5 140

31 +238 - 16 - 90 - 77.4 62.97 99 137 4.3 26.4 34

M.G. 6 79.90 87 134 6.8 19.5 132

9 - 21 + 15 - 11 - 2.4 77.48 91 139 10.8 10.8 248

F. B. 10 45.10 85 131 4.2 25.5 80

18 + 32 -183 - 29 - 53.3 39.60 104 143 4.0 25.8 72

22 - 53 - 89 - 40 - 26.6 39.06 102 138 4.0 25.6 39

D. S. 10 67.13 84 134 6.3 26.5 112

19 -162 -708 -253 - 75.2 59.32 103 141 3.7 18.9 72

24 + 63 -135 + 31 - 30.2 57.78 109 140 4.2 18.9 30

*Totalbalance dataforeachphase^arerecordedattheend ofeachphase, indicatedintimeastheday^from^onset of oliguria.

Waterexchange

The individual factors which determined the net water

exchange (and hence AW as calculated in Equation ⁶ above) ^were calculatedas follows:

"Sensible" water loss (SL) ^was ^measured âs ^the ^sum of water in urine, feces, vomitus, ând blood drawn for analysis. "Insensible" water loss (IW) ^{in these} patients included water vaporized ^from lungs and skin, ând ^was taken as equivalent^to⁹¹ percentof theinsensible weight

loss (IL) ^as ^measured (Equation4) (9).

Available water included exogenouswater administered (H20.) plus endogenous ^water ^from ^oxidation (H20--)

of the metabolic mixture and preformed ^water (H,O,t)

releasedin the catabolism of tissues. Waterof oxidation was calculated (14) ^as:

H20--=^{=0.6 C}⁺^1.07 ^{F +}^0.43 ^P ⁽¹⁴⁾ and preformed ^water (pre-existing intracellular water released with cellularcatabolism) ^as:

H2OPf⁼18.75 bW', (15)

where bN' is the balance of nitrogen corrected for the change ⁱⁿ body fluid urea nitrogen (Equation 2) ^{and the} factor 18.75is6.25X3.0 (it beingassumed thatthereare

approximately 3 parts of water to 1 part of protein ⁱⁿ muscle, the bulk tissue of thebody).

The amount of exogenous water in ^excess of meas-

ured "sensible" water loss, ^{which is} required ^to ^main-

tain a normal ratio of body water to total body solids, (H20e'), is the difference between the insensible water loss and the amount of water available endogenously:

H20.1'

⁼

IW

^-

(H,O.2

⁺H20p). ⁽¹⁶⁾

RESULTS

Observed data are recorded in Tables II and III.5 Chloride balance ^was

uniformly negative

during

^{the latter} part ^of

oliguria,

^{as was} ^sodium

6Complete protocol ^of representative ^case ^is presented

in TableVI (Appendix).

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balance except in case M. G. In Phases II and III chloride balance ^was less negative ^or ^more positive than sodium balance, a reflection of ex-

cessive urinary sodium loss during diuresis, since generally sodium intake exceeded chloride intake.

Potassium and nitrogen balances were predomi- nantly negative. Body weight fell ^an average of 0.27 kilogram ^per day during Phase I, 0.62 kilo-

gram per day during Phase II, and 0.26 kilogram

perdayduring Phase III. The increase in weight loss during early diuresis correlates well with increasing loss of total body water at this time

(seebelow).

Derived data ^are presented in Table IV. For the sake of brevity these values are recorded as

daily ^averages and standard deviations for each phase, all individual values having been corrected

to astandard body surface areaof 1.68 sq. meters

(themean forthis^group ofpatients)."

A. Metabolic mixture

Caloric expenditure averaged approximately 2,500 calories ^per day with little variation from patienttopatientorfrom phasetophase. Theav- erage amounts of protein, carbohydrate, and fat burned ascalculated by the methods described are

enumerated. During Phase I fat constituted the major portion of the metabolic mixture and this

represents primarily endogenous fat, since little

exogenous fat ^was given. The amount of fat ca-

tabolized decreased progressively during Phases

Body ^surface ^area ⁱⁿ sq. meters⁼Wt' Ht"!6X

0.007184 (after DuBois andDuBois [15]).

TABLE IV

Derived data: Mean*daily values formetabolicmixture, changesinbodycompositionand

exchanges of electrolytes^andwater

Phaset

It II III

mean s.d. mean s.d. mean s.d.

A. Metabolic mixture

CHO burned gm./24 hr. 113 :1: 18 183 + 42 194 1: 28

Protein burned gm./24 hr. 42 :1: 19 52 1: 21 59 ^4- 15

Fatburned gm./24 hr. 201 + 32 177 1:103 140 :1: 66

Caloricexpenditure cal./24 hr. 2,405 4:1150 2,610 ^:1:402 2,339 :4:263

B. Changes in body composition

AFat gm./24 hr. -195 :41 49 -156 41 89 -110 4: 90

AW ml./24 hr. - 54 1:327 -435 1:241 - 59 :1:145

AECI ml./24 hr. - 70 :1:101 -242 :4:197 ^- 33 -4119

Al ml./24hr. + 16 +261 ^-193 4:1193 - 26 4-104

ASolids gm./24 hr. - 30 :1 17 -64 :1 24 - 76 ::36

ALBM gm./24 hr. - 83 :1:330 -499 :i:272 -135 =1169

C. Electrolyte exchanges

ACI mEq./24hr. - 16 -:i 2 - 20 a 28 + 12 ⁴ 22

ANaE mEq./24 hr. - 15 4 10 - 30 4: 31 - 4 :1: 17

ANax mEq./24hr. + 1 14 9 - 13 :1 18 ^- 12 1 17

AKE mEq./24hr. + 4 1:7 - 2 : 2 :10 +11

AKi mEq./24 hr. - 12 :1 12 - 18 :: 14 - 9 4- 10

AKI' mEq./24hr. + 11 : 8 + 5 :111 + 12 :1:12

D. Water exchanges

Exogenous intake (H20IN) ^{ml./24 hr.} 1,028 :1:441 2,780 :1:470 3,530 :1:646

Waterofoxidation (H200.) ^{ml./24 hr.} ³⁰³ ^{:1 30} ³³² ^{:1 96} ²⁹¹ ^:1 ⁶⁷

Endogenouspreformed (H20,f) ^{ml./24 hr.} ¹²⁴ ^: ⁷⁵ ¹³² ^: ⁵⁷ ¹⁰⁹ ^{:1: 45}

Insensibleloss (IW) ml./24 hr. 981 :1:141 1,042 :1:278 954 :41206

Sensible loss(SL) ml./24 hr. 296 4:113 2,452 :41623 3,056 :41579

Waterrequiredin excess of SL ml./24 hr. 554 4:1104 587 :1:226 554 :1:156 (IW^-H2001 ^- H20,)

* Mean ofindividualvalues for all patients in each phase corrected to standard body surface area of 1.68 sq. meters (theaveragebodysurface areafor the group).

tSixpatients studied duringPhaseI, 7 during Phase II, and 6 during Phase III.

tValues refer only to latter part of oliguric phase (average 5 days) since studies were not begun at onset ofoliguria.

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II and III, possibly a reflection of decreasing stores of body fat and/or of increasing exogenous caloric intake. The amount of protein burned averaged approximately 50 grams per day in this series, and the amount of carbohydrate burned was assumed to be equal to that given. (Significant glycosuriawas absent in all patients.)

B. Changes in body composition

The derived data from Table IV (B) are pre- sentedasaverage cumulative changes in Figure 1, the duration of each phase being the mean for the group. Expressedin this manner, 15 per cent of initial body fat, 14 per cent of initial body water, and 12 per cent of initial body solids were lost duringtheentireperiodof study (mean21 days).

Extracellular water was diminished by 25 per cent, and intracellular water by 9 per cent. Expressed indifferent terms, of the mean loss of body weight 34 per cent represented loss of fat, 52 per cent loss ofwater, and 14 per cent loss of solids.

Fat was estimated to constitute a relatively large portion of total body weight in these patients, all but one of whom were clinically obese. Body fat wasdepleted atsteadily decreasing rates through- outtheperiod of study. If therateof endogenous fat catabolism during the early part of Phase I, before studies were initiated, ^can be assumed to beroughly equal to that calculated during the latter part of this phase (195grams per day), thenmean fat loss during the entire period of oliguria could be adjusted upward to 13 per cent of total fat storesand to 23 percentduringallthreephases.

Lean body mass (water and solids) was diminished by an average of 26 per cent during the en- tireperiod of study, accountingfor

approximately

66 percentof thetotal weightloss.

Changes in volume of total body water, extracellular and intracellular water were variable,

70- 60-

50-

40 Kg

30-

20- 10

0-

-4-%

-2%.M.

-8%

Dayfrom onset 8 13 22

Phose ^I 1I

I

^m

Oliguric | Early Late Dturetic

.e5%':

^Fat

25% Ec, Total body

:9% I wated

So1ids

29

FIG. 1. CHANGES IN BODY COMPOSITION IN ACUTE RENAL FAILURE

Mean cumulative changes in 8 patients of body weight, fat, total water, chloride space (E01), non-chloride space (I), and solids, based on the values presented in Table IV (B), and a mean initial body weight of65 kg.

particularly during Phase I. Mean values, however, indicated a depletion of total body water duringeachphase, the rate of loss being approximately eight times greater in Phase II (-435 ml.

per day) than in Phases I and III (-54 and

- 59 ml. per day, respectively). Also during Phase IImore than 50 per cent of the total water loss camefrom the chloride space, representing a mean reduction of 19 per cent of this space com- pared toa meanreductionof 8percentof thenon- chloride space.

Body solids decreased at slow, gradually increasing rates (30, 64, and 76 grams per day ⁱⁿ Phases I, II, and III, respectively). These

TABLE V

Derived data: Estimatedmeanbody composition^at^startof study^{and end}of^PhasesI, II,^andIII, expressedaspercentagesoftotalbody weightandofleanbodymass^*

Time

Start ofstudy End Phase I End Phase II End Phase III

Fat

%wt.

34.8 34.0 35.1 34.7

Water

% wt. %LBM

48.2 73.8 48.8 74.0 47.1 72.5 47.8 73.2

Eci

%wt. %LBM

16.9 25.9 16.9 25.5 14.8 22.7 14.7 22.5

% wt. %LBM

31.3 47.9 32.0 48.5 32.3 49.8 33.1 50.7

*FordeviationseeCakulations.

Solids

% wt. %LBM 17.0 26.2 17.2 26.0 17.8 27.5 17.5 26.8

- -

..e.

, ..^..

-, '.

1:1, ^I

(9)

changes, calculated indirectly from changes in body weight minus changes in body fatand water, were in fair agreement with direct measurements of solids lost in urine and feces, averaging 18, 61, and79gramsperday insuccessive phases.

While the overall average losses of total body fat, water, and solids were appreciable, relatively little change occurred in body composition in terms of the ratio of each compartment to total body weight (Table V). Thus it would appear that the total decrements of fat, water, and solids were roughlyproportional to their respective proportions of the totalbodyweight. Thisgeneraliza- tion does nothold, however, during the early diuretic phase (Phase II) when total body water loss, particularly extracellular fluid loss, was dis- proportionatelygreat.

C. Electrolyte changes

The derived data from Table IV (C) are presented as average cumulative balances in Figure

+1001 Chloride O _

mq. -100]

-200 -300

+100-

Sodium 0

fe

-l00.

-200- -300- -400-

-500

-600

+2001

*1001 Potassim ^o _

f"' -100]

-200j -300

Day fromonset 8

Phose ^I

|Otigurk

total

N

intracellular

extracellular

intracellular

#(corroeced forritrogoe .-extracellular

* total introcellular

13 22 29

Iar

I

^m ^I

Early Late Diuretic

FIG. 2. EXTERNAL BALANCES AND INTERNAL TRANSFERS oFELECTROLYTESINACUTERENALFAILURE Mean cumulative balance of chloride, sodium, and ^potassium, and mean cumulative changes in intracellular and extracellular sodium and potassium, based ^on values presented in Table IV (C).

2. Significant mean negative balances of chloride were observed in the first two phases, and of sodium in all three phases. Maximal rates of negative sodium and chloride balance coincided with maximal rates of negative water balance, during the early diuretic phase. Total average negative sodium balance (- 569 mEq.) exceeded total average negative chloride balance (- 181 mEq.) by 388 mEq. Total average potassium balance was - 288 mEq. Maximum negative daily balance of all three electrolytes occurred during Phase II.

Cumulative chloride balances were: - 82, - 264, and - 181 mEq. in Phases I, II, and III, respectively. Average daily chloride balances in each of these phases were: -16.3 (+ 2.4), ^- 20.3 (±27.7), and + 11.9 (±21.8) mEq., respectively. The mean positive chloride balance in Phase III associated with a persistent slight mean negative extracellular water balance, ac- counted for signicant increases in serum chloride concentration in the majority of these patients.

Maximum daily negative sodium balance occurred during Phase II (-43 mEq.) during which time more than twice as much sodium was lostfrom the chloridespace as from the non-chloridespace. During Phase IIIintracellularsodium losscontinuedatabout the same rate (- 12 mEq./

day) whereas the rate of extracellularsodium loss decreased appreciably.

Overall mean cumulative potassium balances were: -44, - 233, and - 288 mEq. in progres- sive phases, respectively. Negative mean daily potassium balance in Phase II (- 19.9 mEq.) wasapproximately twice that in Phases I and III (- 8.8 and 9.3 mEq.). The less negativebalance in Phase III appears to be related more to increased potassium intake (Table II) than to increasing renal conservation. As could be ex- pected, the change in extracellular balance of potassium was minimal and contributed little to the total balance. Mean total intracellular potassium loss was 285 mEq. while total potassium released through cellular catabolism averaged 477 mEq.

Thus the difference, 192 mEq., represented the average amountofpotassiumtaken upby remain- ingintactcells inexcessofnitrogen,^orthepositive intracellular potassium balance corrected for protein burned.

.... ...% ... ... .

;

OtE9.

1101